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. 2019 Dec 12;9:1403. doi: 10.3389/fonc.2019.01403

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Copyright © 2019 Zheng, Dong, Zhao, Wang, Jiang, Zhang, Zheng and Gu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The mechanism underlying the role of METTL3 in the PI3K/AKT pathway. Overexpression of METTL3 coupled with increased m⁶A level promotes the negative AKT regulator PHLPP2 and inhibits the expression of the positive AKT regulator mTORC2, which subsequently decrease the AKT phosphorylation level and downstream effector. Knockdown of METTL3 can activate the PI3K/AKT pathway by positively regulating the phosphorylation of AKT. METTL3, methyltransferase-like 3; PHLPP2, PH domain leucine-rich-repeat protein phosphatase 2; LEF1, lymphoid enhancer binding factor 1; p70S6K, ribosomal protein S6 kinase B1.